Evidence map›Paper›PMID 28361736›Full record

ReviewMicrobiology spectrum2017

DNA Replication in Mycobacterium tuberculosis.

Zanele Ditse, Meindert H Lamers, Digby F Warner

Open access · greenAbstract readReview
In one paragraph

Review in Microbiology spectrum, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.3field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Integrative transcriptome-based drug repurposing in tuberculosis.bioRxiv : the preprint server for biology · 2025
    Article
  7. Review
  8. Expression ofFrontiers in cellular and infection microbiology · 2025
    Article
  9. Article
  10. Article
  11. An additional proofreader contributes to DNA replication fidelity in mycobacteria.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  12. Regulatory role ofFrontiers in microbiology · 2024
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 3 institutions in 2 countries.

Zanele DitseCentre for HIV and STIs, National Institute for Communicable Diseases of the National Health Laboratory Service, Johannesburg, 2131, South Africa.
Meindert H LamersMedical Research Council Laboratory of Molecular Biology, Cambridge, CB2 0QH United Kingdom.
Digby F WarnerSouth African Medical Research Council (SAMRC)/National Health Laboratory Services (NHLS)/University of Cape Town (UCT) Molecular Mycobacteriology Research Unit, Department of Science and Technology (DST)/National Research Foundation (NRF) Centre of Excellence for Biomedical TB Research, Department of Pathology, Faculty of Health Sciences, University of Cape Town, Rondebosch 7700, South Africa.
MRC Laboratory of Molecular Biology · GBNational Health Laboratory Service · ZASouth African Medical Research Council · ZA

Funding

Replisome dynamics in M tuberculosis_linking persistence to genetic resistanceU01HD085531 · NICHD · UNIVERSITY OF CAPE TOWN · PI WARNER, DIGBY FRANCIS, WOODGATE, ROGER · 2015 to 2019
$1.1M
Medical Research Council MC_U105197143NICHD NIH HHS U01 HD085531
6 · The paper itself

Abstract

Faithful replication and maintenance of the genome are essential to the ability of any organism to survive and propagate. For an obligate pathogen such as Mycobacterium tuberculosis that has to complete successive cycles of transmission, infection, and disease in order to retain a foothold in the human population, this requires that genome replication and maintenance must be accomplished under the metabolic, immune, and antibiotic stresses encountered during passage through variable host environments. Comparative genomic analyses have established that chromosomal mutations enable M. tuberculosis to adapt to these stresses: the emergence of drug-resistant isolates provides direct evidence of this capacity, so too the well-documented genetic diversity among M. tuberculosis lineages across geographic loci, as well as the microvariation within individual patients that is increasingly observed as whole-genome sequencing methodologies are applied to clinical samples and tuberculosis (TB) disease models. However, the precise mutagenic mechanisms responsible for M. tuberculosis evolution and adaptation are poorly understood. Here, we summarize current knowledge of the machinery responsible for DNA replication in M. tuberculosis, and discuss the potential contribution of the expanded complement of mycobacterial DNA polymerases to mutagenesis. We also consider briefly the possible role of DNA replication-in particular, its regulation and coordination with cell division-in the ability of M. tuberculosis to withstand antibacterial stresses, including host immune effectors and antibiotics, through the generation at the population level of a tolerant state, or through the formation of a subpopulation of persister bacilli-both of which might be relevant to the emergence and fixation of genetic drug resistance.

Indexed as

Adaptation, BiologicalDNA ReplicationMutationAnimalsHumansMycobacterium tuberculosis

Identifiers

PMID28361736
PMCPMC5507077
OpenAlexW2602926474

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.